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Biomedical subjects

K Ando

Publications and source records attributed to K Ando.

At least 163 records · Page 9Linked to original sources
PubMed1999

Taxonomic re-evaluation of 'Nocardiopsis' sp. K-252T (= NRRL 15532T): a proposal to transfer this strain to the genus Nonomuraea as Nonomuraea longicatena sp. nov.

Re-evaluation of the taxonomic position of strain K-252T, which produces the compound K-252a, showed that the strain does not belong to the genus Nocardiopsis suggested previously. Strain K-252T formed aerial mycelia with long spore chains, and hyphal fragmentation was not observed. The cell wall chemotype of the strain was III/B, the major menaquinone was MK-9 (III, VIII-H4), the phospholipid pattern was PIV and the major cellular fatty acids were 10Me-C17:0, iso-C16:0 and C16:0. Phylogenetic analysis of the 16S rRNA sequence showed that strain K-252T was clustered in the Nonomuraea group. Furthermore, on the basis of DNA-DNA reassociation and phenotypic data, strain K-252T (= NRRL 15532T) was classified as a new species of the genus Nonomuraea. This strain is proposed as Nonomuraea longicatena sp. nov.

Actinomycetales↗
PubMed1999

Chromosome breakage and cell lethality in human hepatoma cells irradiated with X rays and carbon-ion beams.

Prediction of radiosensitivity would be valuable for heavy-ion radiotherapy. Premature chromosome condensation (PCC) technique has been a potential predictive assay in photon radiotherapy, but has not been investigated for hepatomas receiving heavy ions. Two human hepatoma cell lines, i.e., HLE and HLF, were irradiated with either 290 MeV/u carbon ions or 200 kVp X rays. Cell lethality was assayed by colony formation and compared with the unrejoined fraction of chromatin breaks as measured by PCC technique. Carbon ions at linear energy transfer (LET) of 76 keV/micron produced cell death more effectively than those of 13 keV/micron and X rays. For the cell killing, the relative biological effectiveness (RBE) of 13 and 76 keV/micron carbon ions compared with X rays was 1.10-1.24 and 2.57-2.59, respectively. Mean number of chromosomes in HLE and HLF cells was similar to each other, i.e., 60.48 and 60.28. RBEs for chromatin breaks of 13 and 76 keV/micron carbon ions were 1.30-1.31 and 2.64-2.79, respectively. A strong correlation between unrejoined chromatin breaks and cell killing for human hepatoma cells was observed irrespective of radiation quality. We conclude that PCC provides a potential predictor for the radiosensitivity of individual hepatoma that are treated with photon as well as heavy ion irradiation.

Carbon↗
PubMed1999

Cell cycle and LET dependence for radiation-induced mutation: a possible mechanism for reversed dose-rate effect.

A previous study of the mutagenic action of 252Cf radiation in mouse L5178Y cells showed that the mutation frequency was higher when the dose was chronic rather than acute, which was in sharp contrast to the effects reported for gamma-rays (Nakamura and Sawada, 1988). A subsequent study using synchronized cells revealed that the cells at the G2/M stage were uniquely sensitive to mutation induction by 252Cf radiation but not to gamma-rays (Tauchi et al., 1993). A long phase cell population was first subjected to conditioning gamma or 252Cf radiation doses at different dose-rates. The cell cycle distribution of these cells was then observed, and they were then exposed to 252Cf radiation, and the mutation rate was determined. The G2/M fraction increased by 3- to 4-fold when the conditioning doses (2 Gy of gamma or 1 Gy of 252Cf radiation) were delivered chronically over 10 h, but only slightly when the same doses were delivered over a 1 h period or less. Subsequent 252Cf irradiation gave higher mutation frequencies in the cells pre-irradiated with gamma-rays over a protracted period of time than in those exposed with the higher dose-rate gamma-rays. These results suggest that the radiation-induced G2 block could be at least partly (but not totally) responsible for this reverse dose-rate effect (Tauchi et al. 1996). Possible factors which cause the hyper-sensitivity of G2/M cells to mutation induction by neutrons will be discussed.

Animals↗
PubMed1999

Expression of Ah receptor and dioxin-related genes in human uterine endometrium in women with or without endometriosis.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been suggested as a possible etiologic factor for endometriosis, a condition in which endometrium-like tissues are present outside the uterus. The prevailing view pertaining to the origin of endometriotic cells is that they are from eutopic endometrial cells which regurgitate through fallopian tubes. In order to get insight into the possible involvement of TCDD in the pathogenesis of endometriosis, we suspected that TCDD may act differently on the endometrium with or without endometriosis. To address this, we examined the presence of messenger RNAs of arylhydrocarbon receptor (AhR), AhR nuclear translocator (Arnt) and two dioxin-responsive genes, cytochrome P-450 1B1 (CYP1B1) and downstream of tyrosine kinases (p62(dok)), in the endometrium of women with or without endometriosis using semi-quantitative reverse transcription-polymerase chain reaction. All the genes were expressed throughout the menstrual cycle. The expression level of p62(dok) was higher in the proliferative phase than in the secretory phase. In contrast, the expression levels of AhR, Arnt and CYP1B1 seemed to be constant during the cycle. In terms of the comparison between non-endometriosis and endometriosis group, the mRNA levels of AhR, Arnt, CYP1B1 and p62(dok) were essentially similar. Interestingly, AhR mRNA level was significantly lower in smokers than in non-smokers. Based on the regression analysis, significant linear and positive correlations were observed between AhR and Arnt mRNA levels, and between Arnt and p62(dok) mRNA levels. In summary, expression of AhR and dioxin-related genes in the endometrium did not differ in women with or without endometriosis.

Adult↗
PubMed1999

Improvement of multiple facial gingival recession by non-surgical and supportive periodontal therapy: a case report.

We report a case of multiple facial gingival recession which was improved by non-surgical and supportive periodontal therapy. The patient, a 28-year-old Japanese woman, presented for treatment of multiple facial gingival recession ranging from 1 to 4 mm on teeth 5 through 12 and 19 through 30. Periodontal plastic surgery to cover the exposed multiple root surfaces was suggested. However, because of emotional problems, the patient did not wish to undergo the procedures and instead accepted non-surgical periodontal therapy including oral hygiene instruction, scaling, and root planing. The exposed root sites were monitored at periodic maintenance visits, and gradual improvement through a coronal increase of the gingival margin was noted. The possible etiologic factors and healing process associated with this case are discussed.

Adult↗
PubMed1999

Estriol add-back therapy in the long-acting gonadotropin-releasing hormone agonist treatment of uterine leiomyomata.

The hypoestrogenic state induced by gonadotropin-releasing hormone agonists (GnRHa) has been shown to be effective in the treatment of uterine leiomyomas but to induce bone loss. Estriol has been described to be a weak and short-acting estrogen without an increased risk of endometrial proliferation and hyperplasia. The purpose of this study was to evaluate whether treatment of uterine leiomyomata with GnRHa plus oral estriol add-back therapy could prevent bone loss, without deteriorating the therapeutic effect of GnRHa. Twelve premenopausal women with symptomatic uterine leiomyomas were randomized to receive either leuprolide acetate depot alone at a dose of 3.75 mg s.c. every month for 6 months (non add-back group; n = 6), or GnRHa for 6 months plus oral estriol 4 mg/day for 4 months commencing with the third GnRHa injection (add-back group; n = 6). In the add-back group, leiomyoma volume, as measured by transvaginal ultrasound, decreased to 59.1% of baseline at 2 months of GnRHa therapy with no significant change in size during the remaining treatment period. In contrast, it decreased to 31.3% of pretreatment size at the end of treatment in the non add-back group. The levels of bone metabolic markers such as CrossLaps, deoxypyridinoline, osteocalcin and bone-specific alkaline phosphatase, increased significantly throughout the treatment in the non add-back group, whereas they were suppressed by the add-back therapy. The bone mineral density of lumbar spine (L2-L4) as measured by dual-energy X-ray absorptiometry decreased significantly by 7.5% at the end of treatment in the non add-back group, but did not change significantly in the add-back group. In conclusion, GnRHa plus estriol add-back therapy might be considered for long-term treatment of uterine leiomyomata.

Absorptiometry, Photon↗
PubMed1999

RP-1551s, a family of azaphilones produced by Penicillium sp., inhibit the binding of PDGF to the extracellular domain of its receptor.

Nine azaphilones designated RP-1551-1, -2, -3, -4, -5, -6, -7, -M1, and -M2 were isolated from the culture broth of Penicillium sp. SPC-21609 as inhibitors of PDGF binding to its receptor. RP-1551s inhibit the binding of PDGF AA to the extracellular domain of PDGF alpha-receptor with IC50 values ranging from 0.1 to 2 microM without affecting PDGF BB binding to the extracellular domain of PDGF beta-receptor. PDGF binding was not restored after the PDGF alpha-receptor extracellular domain was washed in an attempt to remove the RP-1551-1 bound to the receptor. This result suggests that RP-1551-1 may irreversibly interact with the PDGF alpha-receptor. Since many azaphilone compounds possess high reactivity with an amino group, RP-1551-1 may prevent PDGF AA binding by reacting with amino groups on the alpha-receptor extracellular domain.

Anti-Bacterial Agents↗
PubMed1999

[CT diagnosis of hyperdense intracranial neoplasms: review of the literature].

In contrast to typical astrocytic tumors that show hypodense areas on computed tomographic images, some intracranial tumors show hyperdense areas on CT images. The major reasons for hyperdensity on CT images are hypercellular lesions, intratumoral calcification, and intratumoral hemorrhage. Malignant lymphomas, germinomas, and medulloblastomas show homogeneous hyperdensity on CT images because of their hypercellularity. Tumorous lesions such as subependymal giant cell astrocytomas, oligodendrogliomas, ependymomas, central neurocytomas, craniopharyngiomas, and meningiomas often present with hyperdense calcified lesions on CT images. Intratumoral hemorrhage also causes hyperdensity on CT images, and is often associated with metastatic brain tumors, glioblastomas, pituitary adenomas, and rarely with any of the other intracranial tumors. Although magnetic resonance imaging is now the major diagnostic tool for diseases of the central nervous system, the first imaging studies for patients with neurologic symptoms are still CT scans. Hyperdense areas on CT images are a clue to making an accurate diagnosis of intracranial neoplasms.

Adult↗
PubMed1999

Telomere stability is frequently impaired in high-risk groups of patients with myelodysplastic syndromes.

Genomic instability induces an accumulation of genetic changes and may play a role in the pathogenesis of myelodysplastic syndromes (MDS). To clarify the possible association between genomic instability and clinical outcome in MDS patients, we compared telomere dynamics to the recently established International Prognostic Scoring System (IPSS) risk groups for MDS. We measured the terminal restriction fragments (TRFs) of 93 patients with MDS at the time of diagnosis, and telomerase activity was analyzed in 62 patients with MDS using the PCR-based telomeric repeat amplification protocol (TRAP) assay. A total of 53 of 93 MDS patients had TRFs within the age-matched normal range, and the remaining patients showed shortened TRFs (35 patients) or elongated TRFs (5 patients). MDS patients with shortened TRFs had a significantly low hemoglobin concentration (P = 0.04), a high percentage of marrow blasts (P = 0.02), and a high incidence of cytogenetic abnormalities (P < 0.05). The incidence of leukemic transformation was significantly high in patients with shortened TRF length (P < 0.05). In addition, patients with shortened TRF length were frequently seen in the IPSS high-risk group (P < 0.01). Most of the MDS patients had normal-to-low levels of telomerase activity, suggesting that changes in TRF length rather than telomerase activity may more accurately reflect the pathophysiology of MDS. MDS patients with shortened TRF length had a very poor prognosis (P < 0.01), suggesting that telomere dynamics may be linked to clinical outcome in MDS patients. Thus, an abnormal mechanism of telomere maintenance in subgroups of MDS patients may be an early indication of genomic instability. This study demonstrates that telomere stability is frequently impaired in a high-risk group of MDS patients and suggests that, in combination with the IPSS classification system, measurement of TRFs may be useful in the future to stratify MDS patients according to risk and manage the care of MDS patients.

Acute Disease↗
PubMed1998

A combination of semiquantitative telomerase assay and in-cell telomerase activity measurement using exfoliated urothelial cells for the detection of urothelial neoplasia.

BACKGROUND: Telomerase is a ribonucleoprotein that synthesizes telomeres. It is detected in more than 85% of samples obtained from cancer tissues, including urologic neoplasia. The authors determined telomerase activity semiquantatively and in-cell telomerase activity in exfoliated urothelial cells obtained from urologic neoplasia specimens. The goal of this study was to provide additional information regarding a noninvasive approach to the detection of urologic neoplasia. METHODS: The authors used voided urine from 23 patients with urologic neoplasia, 2 patients with nonmalignant urologic disorders, and 10 normal individuals. Semiquantative determination of telomerase activity was performed using a fluorescence-based telomeric repeat amplification protocol (TRAP), and telomerase activity at the cellular level was determined by an in situ TRAP assay. RESULTS: The fluorescence-based TRAP assay detected urinary telomerase activity in samples from 10 of 13 patients with urologic neoplasia before treatment, whereas urinary cells obtained from 3 of 10 patients (including 1 patient with relapse) during or after treatment had detectable telomerase activity. In contrast, the in situ TRAP assay detected telomerase positive cells in samples from 11 of 13 patients before treatment and 6 of 10 patients during or after treatment. Of note was a dissociation of the results of the fluorescence-based TRAP assay and those of the in situ TRAP assay for some patients. Some patients for whom telomerase activity was not detected with the fluorescence-based TRAP assay had a low frequency of telomerase positive cells in their urine. CONCLUSIONS: A combination of semiquantative analysis and an in situ TRAP assay to detect telomerase positive cells might be a useful tool in the identification and monitoring of patients with urothelial neoplasia.

Adult↗
PubMed1998

Enforced CDK4 expression in a hematopoietic cell line confers resistance to the G1 arrest induced by ionizing radiation.

In hematopoietic cells, gamma-irradiation causes a p53-dependent transient G1 phase cell cycle arrest. Various extracellular growth inhibitory signals elicit G1 arrest by targeting CDK4. Here we show that in a myeloid cell line, 32D cl 3, enforced expression of CDK4, but not cyclins D2 nor D3, overrides the gamma-irradiation-induced G1 arrest. CDK4 does not confer resistance to the radiation-induced G2 block observed in parental cells. Ectopic expression of CDK4 overcomes the ionizing radiation-induced inhibition of CDK4 and CDK2 kinase activity. The levels of CDK4 protein do not change after exposure to ionizing radiation in either parental cells or those overexpressing CDK4. Ionizing radiation induces the expression of both p53 and p21, and in cells constitutively synthesizing exogenous CDK4, the return of p53 protein levels to baseline is prolonged. Increased levels of p21 are found associated with CDK4, and not CDK2, in the lines overexpressing CDK4, compared to the parental line, after exposure to ionizing radiation. Enforced expression of CDK4 may therefore overcome a gamma-irradiation-induced G1 arrest through the titration of the CDK inhibitor p21 allowing both CDK4 and CDK2 to remain active.

Animals↗
PubMed1998

Evidence for mRNA expression of vascular endothelial growth factor by X-ray irradiation in a lung squamous carcinoma cell line.

Vascular endothelial growth factor (VEGF) is a multipotent cytokine which plays an important role in various angiogenic conditions as well as in some tumor behaviors. Here we examined the induction of VEGF mRNA by X-ray irradiation in a lung squamous cell carcinoma cell line (RERF-LC-AI). Irradiating the cells with 15 Gy X-rays significantly increased the mRNA expression up to 2.5-fold of control at a post-irradiation time of 16-24 h. The induction of VEGF mRNA by X-ray irradiation was completely blocked by treating cells with either genistein (Src tyrosine kinase inhibitor) or H7 (protein kinase C inhibitor). This suggests that the mechanism of induction might be concerned with the pathway which triggers Src tyrosine kinase of the cell surface and the protein kinase C pathway.

Antineoplastic Agents↗
PubMed1998

Purification and characterization of a thrombin inhibitor from the salivary glands of a malarial vector mosquito, Anopheles stephensi.

A coagulation inhibitor was identified and isolated from the salivary glands of a malarial vector mosquito, Anopheles stephensi. The salivary gland extract prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT) in assays with human plasma. The inhibition assay of the factors in the coagulation cascade by using synthetic chromogenic substrates showed that the anticoagulant in the mosquito salivary glands is a thrombin inhibitor, but not an inhibitor of factor Xa. The anticoagulant was purified to homogeneity from the mosquito thorax which contains the salivary glands by means of a combination of thrombin affinity and anion exchange chromatography. All of the anticoagulant activity was recovered from the fraction bound to the thrombin affinity column and no activity was detected in the unbound fraction. This result indicated that the thrombin inhibitor is the sole anticoagulant in the salivary glands of A. stephensi. This also suggested a noncovalent, reversible interaction between thrombin and its inhibitor. Size exclusion chromatography and SDS-PAGE estimated the molecular weight of the inhibitor as 45 kDa.

Animals↗
PubMed1998

Involvement of Fas-mediated apoptosis in the hematopoietic progenitor cells of graft-versus-host reaction-associated myelosuppression.

The influence of graft-versus-host (GVH) reaction on the host hematopoietic cells clinically manifests itself both as adverse reactions in transfusion-associated GVH disease (GVHD) and as a therapeutic graft-versus-leukemia (GVL) effect in either donor lymphocytes transfusion (DLT) or allogeneic bone marrow (BM) transplantation. We examined the effect of GVH reaction on the host hematopoiesis in the murine parent-into-F1 (P1 --> F1) model of GVHD. The systemic transfer of 5 x 10(7) of C57BL/6 (B6) splenocytes into (B6xDBA/2)F1 mice (BDF1), which results in acute GVHD, reduced the peripheral blood cell counts, the number of BM cells, and colony-forming unit-granulocyte macrophage (CFU-GM), whereas the injection of 10(8) of DBA/2 cells into BDF1, which results in chronic GVHD, did not affect hematopoiesis 2 weeks after the transfer. To clarify the mechanism of such myelosuppression, we examined the Fas expression in both hematopoietic progenitor cells as well as whole BM cells. The Fas expressions in each fraction significantly increased in BDF1 mice 2 weeks after the induction of acute GVHD, whereas no such effects were observed in the BDF1 mice with chronic GVHD. Furthermore, when such BM cells were incubated with anti-Fas antibody (Jo2), which induces apoptosis through Fas, the fraction of apoptotic cells increased and the number of CFU-GM decreased significantly. The in vivo administration of neutralizing anti-FasL antibody into BDF1 mice receiving with B6 spleen cells thus protected the host mice from BM failure. These results indicate that the functional expression of Fas on hematopoietic cells plays an essential role in the myelosuppressive effect of GVHD.

Animals↗
PubMed1998

An increase in [3H]QNB binding by proton-beam irradiation in intact rat brain: an apparent positive cooperativity of binding.

After focal irradiation of rat brains with a beam of proton (dose, 30 Gy), [3H]quinuclidinyl benzilate (QNB) binding, both in vitro and in vivo, was measured, using either autoradiographic or tissue-dissection methods. No changes in in vitro [3H]QNB binding were seen in autoradiograms of brain slices from irradiated rat. The irradiated side of the brain showed a significant increase in [3H]QNB binding in vivo in the striatum and cerebral cortex 24 h after irradiation. This increase in binding was transient, and had almost disappeared 2 weeks after irradiation. These results indicate that early changes in receptor function as a results of radiation damage are only detected in in-vivo conditions. In the striatum of the intact rat brain, an apparent positive cooperativity of binding was observed, which was more pronounced on the irradiated side.

Animals↗